Abstract
We have used primary cultures of male rat anterior pituitary cells to characterize two effects of pretreatment with 17β-estradiol: 1) the ability to overcome the inhibition of PRL accumulation in the medium (production) by dihydroergocryptine, a dopamine agonist, and 2) the stimulation of PRL production. Medium containing untreated serum contained 20 pm estradiol (E2). In this medium, incubation with dihydroergocryptine for 12 or 24 h caused half-maximal inhibition of PRL production at 150 pm; maximal inhibition reduced values to 32% of the control value. Pretreatment with 50 nm E2 for 5 days decreased the maximal inhibition of PRL production caused by dihydroergocryptine to 65% of control values, with little or no effect on the concentration of ergot which caused half-maximal inhibition. In addition, pretreatment with 50 nm E2 did not increase basal PRL production. Medium containing charcoaltreated serum was calculated to contain less than 2 pm E2. In this medium, dihydroergocryptine caused half-maximal inhibition of PRL production at 30 pm; maximal inhibition was reduced to 32% of controls. E2 decreased the maximal inhibition of PRL production to 60% of controls and caused an increase in the halfmaximal concentration of dihydroergocryptine which ranged between 7- and 32-fold, with an average of 18-fold. With most batches of treated serum, but not all, E2 stimulated basal PRL production 1.6- to 5.9-fold. The E2 effect on the response to dihydroergocryptine was maximal at 2 days; the E2 effect on basal PRL production was still increasing between 2–5 days of exposure. Both effects were maximal at 50 pm E2. Diethylstilbestrol (5 nm) showed the same effects as E2) but 50 nm progesterone, testosterone, or hydrocortisone did not. Therefore, even though both effects of E2 do not necessarily occur together, both effects are pharmacologically specific and occur at similar doses and times after pretreatment. (Endocrinology106: 1108, 1980)